Effects of Glut1 gene silencing on proliferation, differentiation, and apoptosis of colorectal cancer cells by targeting the TGF‐β/PI3K‐AKT‐mTOR signaling pathway

2017 ◽  
Vol 119 (2) ◽  
pp. 2356-2367 ◽  
Author(s):  
Xue‐Liang Wu ◽  
Li‐Kun Wang ◽  
Dong‐Dong Yang ◽  
Ming Qu ◽  
Yong‐Jiang Yang ◽  
...  
Keyword(s):  
Colorectal Cancer ◽  
Gene Silencing ◽  
Cancer Cells ◽  
Signaling Pathway ◽  
Mtor Signaling ◽  
Mtor Signaling Pathway ◽  
Colorectal Cancer Cells ◽  
Glut1 Gene

scholarly journals DHOK Exerts Anti-Cancer Effect Through Autophagy Inhibition in Colorectal Cancer

2021 ◽  
Vol 9 ◽  
Author(s):  
Yuhan Shu ◽  
Xin Sun ◽  
Guiqin Ye ◽  
Mengting Xu ◽  
Zhipan Wu ◽  
...  
Keyword(s):  
Colorectal Cancer ◽  
Cancer Cells ◽  
Signaling Pathway ◽  
Mammalian Target Of Rapamycin ◽  
Mtor Signaling ◽  
Dependent Manner ◽  
Mtor Signaling Pathway ◽  
Eurycoma Longifolia ◽  
Anti Cancer ◽  
Lc3 Puncta

DHOK (14,15β-dihydroxyklaineanone) is a novel diterpene isolated from roots of Eurycoma longifolia Jack, a traditional herb widely applied in Southeast Asia. It is reported that DHOK has cytotoxic effect on cancer cells, but its anti-cancer mechanism has still been not clear. In our study, we first observed that DHOK inhibits cell proliferation of colorectal cancer cells in a time- and dose-dependent manner. Next, we performed transcriptome sequencing to identify the targets of DHOK and found that autophagy-related signaling pathways are involved under DHOK treatment. Indeed, in DHOK-treated cells, the level of autophagosome marker LC3 and the formation of GFP-LC3 puncta were decreased, indicating the reduction of autophagy. Moreover, confocal microscopy results revealed the lysosomal activity and the formation of autolysosomes are also inhibited. Our western blotting results demonstrated the activation of mammalian target of rapamycin (mTOR) signaling pathway by DHOK, which may be attributed to the enhancement of ERK and AKT activity. Functionally, activation of autophagy attenuated DHOK-caused cell death, indicating that autophagy serves as cell survival. In xenograft mouse model, our results also showed that DHOK activates the mTOR signaling pathway, decreases autophagy level and inhibits the tumorigenesis of colon cancer. Taken together, we revealed the molecular mechanism of DHOK against cancer and our results also demonstrate great potential of DHOK in the treatment of colorectal cancer.

scholarly journals Curcumin Regulates the Progression of Colorectal Cancer via LncRNA NBR2/AMPK Pathway

2019 ◽  
Vol 18 ◽  
pp. 153303381987078 ◽  
Author(s):  
Hua Yu ◽  
Yangyang Xie ◽  
Zhendong Zhou ◽  
Zhou Wu ◽  
Xiaoyu Dai ◽  
...  
Keyword(s):  
Colorectal Cancer ◽  
Protein Kinase ◽  
Cancer Cells ◽  
Noncoding Rna ◽  
Glucose Deprivation ◽  
Adenosine Monophosphate ◽  
S Phase ◽  
Mtor Signaling ◽  
Mtor Signaling Pathway ◽  
Colorectal Cancer Cells

Objective: To identify the effect of curcumin on tumor suppression and the possible molecular pathways involved. Methods: The expression of long noncoding RNA neighbor of BRCA1 lncRNA 2 (NBR2) was quantified using reverse transcription-polymerase chain reaction on cultured colorectal cancer cells. Next, we used Western blot to measure the activation of adenosine monophosphate-activated protein kinase and mechanistic target of rapamycin kinase (mTOR) signaling molecules. Both cell proliferation and viability were measured via MTT assay, and the cell ratio and S phase were detected by BrdU assay. Colorectal cancer cells were pretreated with curcumin or transfected with shNBR2 or adenosine monophosphate-activated protein kinase inhibitor Compound C to examine the molecular pathway involved. Results: Current data showed that glucose deficiency increased the expression of NBR2 in colorectal cancer cells, and NBR2 knockdown affected the progression of colorectal cancer cells under glucose starvation conditions. When NBR2 was silenced in the treated colorectal cancer cells, the proliferation, the clone formation, and the percentage of S-phase cells suppressed by glucose deprivation were compromised. Furthermore, NBR2 knockdown could suppress glucose deprivation-induced adenosine monophosphate-activated protein kinase activation plus mTOR inactivation. Similarly, when colorectal cancer cells were treated with curcumin, the expression of NBR2 was significantly increased. NBR2 knockdown reversed curcumin-suppressed proliferation, clone formation, and the percentage of S-phase colorectal cancer cells. Furthermore, NBR2 knockdown abolished curcumin-induced activation of adenosine monophosphate-activated protein kinase and inactivation of the mTOR signaling pathway. Conclusion: This study revealed a novel mechanism by which long noncoding RNA NBR2 mediates curcumin suppression of colorectal cancer proliferation by activating adenosine monophosphate-activated protein kinase and inactivating the mTOR signaling pathway.

Chaga mushroom extract induces autophagy via the AMPK-mTOR signaling pathway in breast cancer cells

2021 ◽  
pp. 114081
Author(s):  
Min-Gu Lee ◽  
Yun-Suk Kwon ◽  
Kyung-Soo Nam ◽  
Seo Yeon Kim ◽  
In Hyun Hwang ◽  
...  
Keyword(s):  
Breast Cancer ◽  
Cancer Cells ◽  
Signaling Pathway ◽  
Breast Cancer Cells ◽  
Mtor Signaling ◽  
Mtor Signaling Pathway ◽  
Mushroom Extract

Angiogenin interacts with ribonuclease inhibitor regulating PI3K/AKT/mTOR signaling pathway in bladder cancer cells

2014 ◽  
Vol 26 (12) ◽  
pp. 2782-2792 ◽  
Author(s):  
Yuan Peng ◽  
Lin Li ◽  
Mengge Huang ◽  
Changzhu Duan ◽  
Luyu Zhang ◽  
...  
Keyword(s):  
Bladder Cancer ◽  
Cancer Cells ◽  
Signaling Pathway ◽  
Mtor Signaling ◽  
Mtor Signaling Pathway ◽  
Ribonuclease Inhibitor ◽  
Bladder Cancer Cells
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